ABSTRACT Notch signaling pathway modulates immune function by regulating T cell development, differentiation, and function. Previous studies from our group have demonstrated that maternal exposure to staphylococcal enterotoxin B (SEB) during pregnancy alters T cell frequencies in offspring. To further investigate the underlying mechanisms, we examined the impact of prenatal SEB exposure on the Notch signaling pathway, a critical regulator of thymic T cell maturation. In this study, pregnant rats were injected with 15 μg SEB on gestational day 16. Thymus tissues were aseptically collected from 14‐day‐old and 3‐month‐old offspring in both the PBS and SEB‐exposed groups. The expression of Notch pathway components—including receptors, ligands, and downstream target genes—was assessed using real‐time PCR and western blot. It was found that prenatal SEB exposure significantly downregulated mRNA and protein levels of Notch receptors and target genes in thymic T lymphocytes in neonatal offspring. Additionally, ligand expression was reduced in thymic stromal cells. Strikingly, this suppression was reversed in adulthood, with SEB‐exposed offspring exhibiting elevated expression of Notch receptors, ligands, and target genes. These results indicate that prenatal SEB exposure transiently inhibits Notch signaling in neonatal thymocytes but leads to a compensatory upregulation in adulthood. This biphasic modulation suggests that prenatal SEB exposure can induce long‐term, dynamic reprogramming of thymic Notch signaling, with potential implications for T cell‐mediated immunity across developmental stages.
Gao et al. (Thu,) studied this question.
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